In Vitro Efficacy Testing Services for Neuroblastoma
Drug R&D Solutions

In Vitro Efficacy Testing Services for Neuroblastoma

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We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Neuroblastoma. Our service enables detailed evaluation of compound efficacy, mechanism of action, and cellular pathway modulation specific to Neuroblastoma cells. Key targets include ALK, MYCN, Trk receptors, and associated signaling pathways such as PI3K/AKT/mTOR and MAPK. We are equipped to assess processes including cell proliferation, apoptosis, neurotrophic signaling, and resistance mechanisms relevant to Neuroblastoma pathogenesis.

Our comprehensive in vitro testing suite encompasses a range of biochemical and cell-based assays designed to interrogate compound activity, target engagement, and pathway modulation in Neuroblastoma models. These methods allow for quantitative analysis of drug potency, target binding, and biological response. Collectively, they provide a robust platform for preclinical candidate assessment.

ATP assay: Measures cellular ATP levels to assess cell viability and cytotoxicity, providing a direct readout of compound-induced cell death or proliferation inhibition in Neuroblastoma cultures.

ATP assay (at 0.01 mM): Evaluates drug effects at low compound concentrations, enabling sensitivity profiling and identification of active agents at near-physiological doses.

ATP assay (at 1 mM): Assesses cytotoxicity at higher compound concentrations to determine maximal efficacy and potential off-target effects.

Chemiluminescent assay: Utilizes luminescence-based detection to quantify specific biomolecules or enzymatic activities, supporting high-sensitivity screening of Neuroblastoma-relevant pathways.

ELISA assay: Employs antibody-based detection to measure proteins, cytokines, or phosphorylated targets, facilitating pathway and biomarker analysis in Neuroblastoma research.

Fluorescence resonance energy transfer (FRET) assay: Detects molecular interactions and conformational changes, enabling real-time analysis of protein-protein interactions or signaling events in Neuroblastoma cells.

Fluorescent polarization assay: Measures binding interactions between small molecules and targets, providing quantitative data on compound affinity and specificity.

Homogeneous Time Resolved Fluorescence (HTRF) assay: Combines fluorescence detection and time-resolved measurement for high-throughput quantification of protein interactions or modifications relevant to Neuroblastoma.

Poly(glutamine/tyrosine) peptide as substrate: Utilized in enzymatic assays to evaluate kinase or protease activity, supporting studies of signaling dysregulation in Neuroblastoma.

RNA assay: Quantifies gene expression changes in response to treatment, enabling assessment of molecular mechanisms and pathway modulation in Neuroblastoma cells.

We measure a comprehensive set of pharmacological parameters to characterize compound potency, efficacy, and mechanism of action in Neuroblastoma models. These metrics are critical for ranking candidates, understanding dose responses, and guiding lead optimization. Accurate determination of these parameters underpins informed decision-making in preclinical drug development.

EC-50: The effective concentration of a compound that produces 50% of its maximal effect, reflecting cellular potency and therapeutic window.

IC-50: The concentration at which a compound inhibits a specific biological or biochemical function by 50%, essential for evaluating inhibitor strength and selectivity.

Kd: The dissociation constant representing the affinity of a compound for its target, a key parameter for understanding binding efficiency.

MIC: The minimum inhibitory concentration required to prevent visible growth of cells or microorganisms, providing a benchmark for compound efficacy.

pIC-50: The negative logarithm of the IC-50 value, offering a standardized and comparable measure of inhibitory potency across different compounds.

Recommended In Vitro Efficacy Tests

Cereblon

Cereblon is a key E3 ubiquitin ligase substrate receptor implicated in neuroblastoma progression and is a therapeutic target for novel drug development. Cereblon testing is essential for screening and optimizing drug candidates. Our service employs advanced assays—including fluorescent polarization, chemiluminescence, HTRF, and FRET—to measure compound binding and activity. Main parameters assessed are EC-50, IC-50, and Kd, providing critical data for selecting potent, specific Cereblon modulators in neuroblastoma therapies.

Pharmacological Activity Material Method Parameter
Cereblon affinity Human enzyme IC-50
Cereblon affinity Recombinant human enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Cereblon affinity Recombinant human enzyme Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Cereblon affinity Homogeneous Time Resolved Fluorescence (HTRF) assay IC-50
Cereblon affinity IC-50
Cereblon, inhibition Fluorescent polarization assay IC-50
Cereblon/Damage-specific DNA binding protein 1 affinity Recombinant human enzyme Fluorescent polarization assay Kd
Cereblon/Damage-specific DNA binding protein 1 interaction, inhibition Recombinant protein Fluorescence resonance energy transfer (FRET) assay IC-50
Protein (CRBN) degradation, induction HEK293T human embryonic kidney cells Chemiluminescent assay EC-50

Dna Topoisomerase I

DNA Topoisomerase I is crucial for DNA replication and cell proliferation in neuroblastoma. Inhibiting this enzyme is a key strategy for neuroblastoma drug development. Our testing service employs a sensitive chemiluminescent assay to evaluate compound efficacy, providing precise determination of minimum inhibitory concentration (MIC). This enables rapid identification of potent Topoisomerase I inhibitors, accelerating preclinical drug discovery for neuroblastoma therapeutics.

Pharmacological Activity Material Method Parameter
DNA topoisomerase I expression, inhibition LoVo human colon adenocarcinoma cells Chemiluminescent assay MIC
DNA topoisomerase I expression, inhibition LoVo human colon adenocarcinoma cells (irinotecan-resistant) Chemiluminescent assay MIC

Epidermal Growth Factor Receptor

Epidermal Growth Factor Receptor (EGFR) plays a key role in neuroblastoma cell proliferation and survival, making it a critical drug target. EGFR testing is essential for evaluating candidate drug efficacy. Our service utilizes advanced ATP assays (0.01 mM and 1 mM), FRET, ELISA, chemiluminescent assays, and poly(glutamine/tyrosine) peptide substrates to determine inhibitory potency. Main parameters measured include IC-50 and pIC-50, ensuring precise assessment of drug activity.

Pharmacological Activity Material Method Parameter
Protein-tyrosine kinase (EGF receptor) (L858R-mutated), inhibition Recombinant enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/C797S-mutated), inhibition Recombinant enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M-mutated), inhibition Recombinant enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M/C797S-mutated), inhibition Recombinant enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (EGF receptor) (L858R/T790M/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (T790M-mutated), inhibition Chemiluminescent assay IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted/T790M-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor) (exon 19-deleted/T790M/C797S-mutated), inhibition IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Human enzyme ATP assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Recombinant enzyme ATP assay (at 0.01 mM) pIC-50
Protein-tyrosine kinase (EGF receptor), inhibition Recombinant enzyme ATP assay (at 1 mM) pIC-50
Protein-tyrosine kinase (EGF receptor), inhibition Recombinant enzyme Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Recombinant enzyme Poly(glutamine/tyrosine) peptide as substrate pIC-50
Protein-tyrosine kinase (EGF receptor), inhibition Recombinant human enzyme ELISA assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Chemiluminescent assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition Fluorescence resonance energy transfer (FRET) assay IC-50
Protein-tyrosine kinase (EGF receptor), inhibition IC-50

Receptor Interacting Serine/Threonine Kinase 2

Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) is implicated in neuroblastoma progression and survival pathways. Testing RIPK2 activity is vital for identifying and optimizing targeted therapies. Our service employs chemiluminescent and ATP assays to accurately measure RIPK2 inhibition, with IC-50 determination as a key parameter to assess compound potency, enabling efficient drug screening and development for neuroblastoma treatment.

Pharmacological Activity Material Method Parameter
Serine/threonine protein kinase (RIPK2), inhibition Recombinant enzyme Chemiluminescent assay IC-50
Serine/threonine protein kinase (RIPK2), inhibition Recombinant human enzyme ATP assay IC-50
Serine/threonine protein kinase (RIPK2), inhibition IC-50

Tumor Necrosis Factor

Tumor Necrosis Factor (TNF) is a key cytokine involved in neuroblastoma progression and therapeutic response. TNF testing is vital for assessing drug efficacy and potential cytotoxicity in neuroblastoma drug development. Our service employs RNA assays to quantify TNF expression, enabling precise evaluation of drug impact. Main parameters, such as Minimum Inhibitory Concentration (MIC), help determine the lowest drug concentration needed to inhibit TNF-mediated tumor activity.

Pharmacological Activity Material Method Parameter
Gene (tumor necrosis factor-alpha) transcription (endotoxin-induced), inhibition Macrophages (bone marrow-derived), human (macrophage colony-stimulating factor-stimulated) RNA assay MIC
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